This is a renewal application to continue the studies started one year ago (NS HL 11169-O1A1) on cerebral hemodynamics and subarachnoid hemorrhage (SAH) and the effect thereon of an alpha adrenergic blockader, a kallikrein inhibitor, and a proteolytic enzyme which is believed tc inactivate the vasospastic elements in blood. To date the primary thrust of most investigations has been directed towards large vessel spasm. Since there is no unanimity on either the correlation between this phenomenon and morbidity and mortality or on hemodynamics and the pathophysiology towards which therapy should be directed, the objectives are: In the experimental SAH monkey model which this laboratory developed, 1) to continue the study of relative roles of the macro versus the microvasculature in the hemodynamic catastrophe by quantitating pre and post venous resistance changes as well as gross angiographic spasm, 2) to quantitate the effects of three different therapeutic approaches (neurogenic, kallikrein inhibition and inactivation of spasmolytic agents) on cerebral hemodynamics, metabolism, morbidity and mortality.